TY  - GEN
T1  - Overactive EGF signaling suppresses a C. elegans pnc-1 egg-laying phenotype independent of known signaling mediators.
AU  - Crook, Matt
AU  - Hanna-Rose, Wendy
DO  - 10.17912/micropub.biology.000482
UR  - http://beta.micropublication.org/journals/biology/micropub-biology-000482/
AB  - NAD+ is an electron carrier and a co-substrate for NAD+-dependent enzymes such as poly(ADP-ribose) polymerases (Bouchard et al. 2003; Sauve 2008). The byproduct of these enzymatic reactions, nicotinamide (NAM), must be salvaged to maintain a readily available NAD+ pool. In Caenorhabditis elegans the nicotinamidase PNC-1 acts both cell autonomously and non-cell autonomously to convert NAM into nicotinic acid (NA), an NAD+ precursor in this organism (Huang and Hanna-Rose 2006; Vrablik et al. 2009; Crook et al. 2014). Loss of PNC-1 function affects NAD+ pathway metabolites in two ways. It results in an increase in NAM, causing necrosis of OLQ and uv1 cells, and an egg-laying phenotype due to reduced muscle function. It also reduces NAD+ levels, resulting in gonad developmental delay and a male mating defect (Huang and Hanna-Rose 2006; Vrablik et al. 2009; Vrablik et al. 2011; Upadhyay et al. 2016).
PY  - 2021
JO  - microPublication Biology
ER  -